emphazing ST-segment and T-wave deviation (ischemic changes)

The heart is a muscular pump that circulates blood
through an animal's body.
A person's heart is typically about the same size as
their fist. The heart consists of four chambers. The upper heart
is the atria (two atrial chambers) and the lower part is the
ventricles (two ventricular chambers). The heart is
mainly comprised of a specialized type
of striated muscle, with properties that function somewhat
differently than skeletal muscle. Heart cells are
connected by gap junctions that allow ions to flow from one cell
to another, allowing for rapid spreading of depolarization. A
collection of heart cells connected in this way constitutes
a syncytium. The heart is composed of two syncytiums:
an atrial syncytium and a ventricular syncytium.

The muscle composing walls
of the heart is call the myocardium. The two
ventricles are separated by the
ventricular septum, which is thick &
muscular toward the bottom, and thick & fibrous at the top.
Under the myocardium is the endocardium, which lines the
chambers of the heart, and which is mainly composed of epithelial
cells. The pericardium is a double-walled sac that
contains the heart and the roots of the great vessels. The
outer wall of the pericardium is composed of dense connective
tissue. The portion of the inner wall of the pericardium
that is in contact with the heart (but not in contact with
the great vessels) is the epicardium. The epicardium
contains the blood vessels supplying blood to heart muscle
(the coronary arteries) as well as nerve fibers.

The veins of the body terminate in two great vessels that empty into the
right atrium: the superior vena cava (from the upper body) and
the inferior vena cava (from the lower body). Blood exits
the heart through the pulmonary artery (which takes
unoxygenated blood to the lungs from the right ventricle) and
through the aorta (which distributes oxygenated blood
to the body from the left ventricle). Oxygenated blood from
the lungs enters the left atrium from the pulmonary vein.
The pulmonary artery is the only artery that carries unoxygenated
blood and the pulmonary vein is the only vein that carries
oxygenated blood.

There is a one-way flow of blood from the atria to the ventricles.
Reverse flow is prevented by the A−V valves: the
tricuspid valve (having 3 flaps or "cusps") on the right
and the mitral (bicuspid) valve on the left. The inner flaps of the
A−V valves have connective tissue attachments ("heart
strings") from muscular mounds on the ventricles that prevent the
flaps from bulging too much into the atria during contraction of the
ventricles. Flow of blood back to the ventricles following ejection
of blood from the ventricles is prevented by the semilunar
valves: the pulmonary valve on the right and
the aortic valve on the left, each of which have three flaps
shaped somewhat like half-moons.

The first heart sound ("lubb") occurs during ventricular
contraction when the mitral valve is closing (beginning of
systole), and the second heart sound ("dupp") occurs
during ventricular relaxation when the aortic valve is closing
(beginning of diastole). The closing of the valves on the right
side of the heart are not so easy to hear. Valves that cannot
close completely can cause murmurs associated with regurgitation
of blood. But murmurs are not necessarily an indication of
valve pathology.

The openings to the right and left
coronary arteries (which
supply blood to the heart) are in the aorta just beyond the cusps
of the aortic semilunar valve. The right coronary artery supplies
the right atrium, right ventricle, and most of the posterior
surface of the left ventricle with blood. The left coronary
artery branches into the left anterior descending artery
(which supplies the anterior surface of the left ventricle)
and the circumflex artery (which supplies the left atrium
and parts of the left ventricle).

The heart pumps blood
in a two-step process. The atria pump blood into the ventricles
and then the ventricles pump blood out of the heart. Chambers
of the heart fill with blood during a relaxation phase (diastole)
and eject blood during a contraction phase (systole).
Atrial systole precedes ventricular systole. The systole and
diastole of the left ventricle correspond to the systolic
(high pressure) and diastolic (lower pressure) phases
of blood pressure in the body.

The right atrium pumps blood from the body into the right
ventricle. The right ventricle pumps blood into the lungs.
The left atrium pumps blood from the lungs into the left
ventricle. The left ventricle pumps blood to the body
through the aorta. This cycling of blood by the heart
is called the cardiac cycle. A couple of YouTube
animations illustrate the cardiac cycle:

The left ventricle has the most powerful musculature
insofar as it must pump blood into the entire body. For
the left ventricle the cardiac cycle can be described
in four phases:

Period of filling — volume increases from about 50 milliliters of blood
to about 120 milliliters of blood, after which the A−V valve
(mitral valve) closes. 70% of ventricular filling occurs passively as
blood flows into the atria and through to the ventricles while the tricuspid
valve is open. Atrial contraction pushes the final 30% of blood into
the ventricle, after which the tricuspid valve closes.

Period of isovolumetric contraction — all valves are closed as
pressure rises from 5 mmHg to 80 mmHg while blood volume remains unchanged.

Period of ejection — the semilunar valve (aortic valve) opens and blood
is ejected into the body. 70% of blood emptying occurs in the first third
of the ejection period as pressure rises to 120 mmHg. Pressure drops
to 100 mmHg during the last two-thirds of the ejection period. (Stroke
volume can double during exercise.)

Period of isovolumetric relaxation — pressure drops to zero after
the aortic valve has closed.

Heart electrical conduction

Depolarization and contraction of cardiac muscle is preceded by depolarization of
the cardiac nerve bundles. Depolarization of the heart is initiated at the
sinus node (the
sinoatrial node)
located on the right atrium. Depolarization is transmitted through
the A−V node (Atrio-Ventricular node), the
A−V bundle (the
Bundle of His),
and then through the ventricles by the Purkinje fibers.

The cardiac cycle is initiated in the sinus node in
the atrium, which causes contraction of the atrial syncytium. The depolarization
is delayed at the A−V node before passing to the A−V bundle
and splitting into a right branch bundle and a left branch bundle, sending
depolarization to the muscle of the right ventricle and the left ventricle,
respectively. The A−V node delay prevents the atria and ventricles
from contracting at the same time. During ventricular contraction the wave
of depolarization in the cardiac muscle moves from the endocardium to the
pericardial surface through the myocardium. Unlike cardiac cells which have
mechanical (contractile) function, the cardiac cells having an electrical
conduction function not only conduct electrical impulses, but spontaneously
generate impulses. In a normal heart it is the cardiac cells of the
sinus node that have the highest rate of spontaneous impulse
generation, which makes the sinus node the ultimate pacemaker of
the electrical system of a healthy heart.

Acetylcholine released from parasympathetic nervous
system fibers (vagus nerve) slows the discharge rate at the sinus node,
and slows the conduction rate through the A−V node. Release
of norepinephrine from the sympathetic
(adrenergic) nervous system has the opposite effect on the heart:
increasing heart rate, force of contraction and blood pressure.
Beta−1 adrenergic receptors in the heart increase
heart rate and contractility. Alpha adrenergic receptors
constrict peripheral blood vessels thereby increasing blood pressure.

Cardiac output is defined to be the amount of blood that
the heart pumps in one minute — typically four to eight
liters per minute. Cardiac output equals stroke volume times
heart rate. Typically it takes one minute for a red blood cell
to travel from the heart, through the arteries, capillaries
& veins, and back to the heart. By age 70 cardiac output
can have declined by about one-third in many people. (The
myocardium can also become more irritable with
aging,
leading to irregular heartbeats).

Normal heart rate for an infant is in the range of 100 to 160
beats per minute. Heart rate typically becomes slower as children
get older. For teenagers and adults, 60 to 100 beats per minute
in considered normal, with slower rates called sinus
bradycardia. Sinus bradycardia can be due to
hypothyroidism,
hypokalemia, beta-blocker drugs or
other drugs/pathologies, or it can be normal for
athletes or people who exercise. About one-third of
normal people under age 25 have heart rates less
than 60 beats per minute. Nearly all athletes have
resting heart rates below 60 beats per minute [AMERICAN
JOURNAL OF EMERGENCY MEDICINE; Wu,J; 24(1):77-86 (2006) and
BRITISH JOURNAL OF SPORTS MEDICINE;
Corrado,D; 43(9):669-676 (2009)]. Sinus
tachycardia generally designates heart rates in
the 101 to 180 beats per minute range. Hyperthyroidism,
caffeine,
and nicotine — as well as fear & anxiety
— are among the possible causes of high
heart rates.

Depolarization of the heart can be monitored with three
electrodes attached to the body: one on each arm and one on
the left leg. Depolarization spreads from the right atrium
(corresponding to the electrode on the right arm) to the
left ventricle (corresponding to the electrode on the
left leg). The electrode on the left arm is neutral.
Additional electrodes provide more sensitive monitoring
of depolarization (see section IV).

Normal electrocardiograms

Potential differences between electrodes are
recorded on a chart known as an
electrocardiogram. Cardiography paper is
divided into small squares that are one millimeter on each
side, and large squares which contain five small squares
on each side. Because cardiography paper moves at 25 millimeters
per second, a width of five large blocks contains one second
of waveforms.

Potential
differences between electrodes record a spreading depolarization.
Complete depolarization or complete polarization is a flat
line (midline, zero millivolts). Five waves corresponding
to upward or downward deflections from zero millivolts
on an ECG chart are designated alphabetically as
P,Q,R,S, and T waves. Sometimes a U wave
(of similar shape to a T wave, but of lower amplitude)
follows the T wave. A U wave is usually seen in people
with low heart rates, and is rarely seen when heart rate is
high. The Q,R, and S waves are grouped together as
the QRS complex. Depolarizations
and repolarizations corresponding to these waves
can be summarized by:

Normal T waves are slightly skewed to the right, rather than being
completely symmetrical. U waves are believed to be a delayed component
of repolarization associated with the T wave [CLINICAL CARDIOLOGY;
Correale,E; 27(12):674-677 (2004)].

Atrial repolarization is obscured by the more
powerful QRS complex. The waves of the QRS complex can be described in more detail:

In conditions of hypothermia, a J wave may occur
at the end of the QRS complex. The end of the QRS complex
(beginning of the ST−segment) is called the J point,
a point of zero voltage associated with the exact time when the wave
of depolarization has completed its passage through the heart.

The Q wave can be enlarged by myocardial infarction. The
R−wave can be enlarged (higher or wider) if the ventricle
is enlarged. The QRS complex is prolonged if the Purkinje
fibers are blocked because a depolarization carried through
ventricular muscle has a much slower conduction velocity.

Heart waveforms seen in an electrocardiogram are the sum resultant
of a variety of electrical heart currents. For the QRS wave, it is
the electrical activity of the left ventricle that dominates. The
QRS wave seen is a 20% residue of cardiac electrical activity,
80% of which has been canceled-out by counterveiling currents.
It seems contradictory that depolarization of the left ventricle
would give positive R waves, whereas repolarization of the
left ventricle gives T waves that are also positive. The
explanation is that the T wave displayed is the resultant
of repolarization of the epicardium, the endocardium and the
myocardium (M-cells). Deploarization occurs from endocardium
to epicardium, whereas repolarization is in the reverse direction.
Epicardial cells have completed repolarization by the middle of
the T wave, and the end of the T wave corresponds to
the completion of repolarization of the M-cells.

Electrocardiography is based on the fact that depolarization in
heart muscle induces electric currents in overlying skin. Electrocardiography
was invented at the beginning of the 20th century by the Dutch
physician/physiologist
Willem Einthoven. Although EKG
abbreviates the Dutch word for ElectroCardioGraphy, the
English abbreviation ECG is now the abbreviation most
commonly in use.

Einthoven used a three-lead system — the standard
limb leads — to which has been added three
augmented limb leads and six chest (precordial) leads
in the modern 12−lead ECG. The term "lead" can be
confusing insofar as the standard limb leads are bipolar
(measure the potential difference between two electrodes)
whereas the others are unipolar (single electrode).
The standard limb leads are:

Lead I : potential difference between the
left arm (positive electrode) and the right arm (negative electrode)

Lead II : potential difference between the
left leg (positive electrode) and the right arm (negative electrode)

Lead III : potential difference between the
left leg (positive electrode) and the left arm (negative electrode)

Note that the left arm is positive relative to the right arm and
negative relative to the left leg. There is redundancy in using
these three bipolar leads insofar as the voltage recorded at
Lead II is the sum of the voltages of the other two
leads (I + III = II).

A positive waveform (positive voltage) is recorded when
depolarization flows from a negative electrode to a positive
electrode. For this reason, Lead II typically gives the canonical
ECG patterns because the flow of depolarization from negative
electrode (right arm) to positive electrode (left leg) matches
the typical alignment of the heart in the chest: sloping
downward toward the left side of the body.

Leads I, II, and III give a view of the heard called
Einthoven's triangle, that divides a 360º circle
centered on the heart into three depolarization axes separated
by 120º. Adding the three augmented limb leads divides the
heart into six depolarization axes separated by 60º.
The augmented limb leads are:

aVR : potential difference between the
right arm [shoulder] (positive electrode) and the center of the heart

aVL : potential difference between the
left arm [shoulder] (positive electrode) and the center of the heart

aVF : potential difference between the
left leg ["foot"] (positive electrode) and the center of the heart

hexaxial system

Note that a = augmented, V = Voltage, and the final letter
designates Right or Left arm, or the left leg (called the left Foot because the
letter L was already used by the Left arm). Since the 1960s it has become
common practice for electrodes of both standard & augmented limb leads to
be placed at locations on the torso (trunk) of the body toward the limbs
rather than on the limbs themselves.

Including both positive & negative directions of depolarization
of both the standard & augmented limb leads gives a 360º circle
divided into twelve 30º sections that is called the
hexaxial reference system. Lead I (pointing
toward the left arm) is taken as the reference for 0º lead
orientation, with increasing positive values in a clockwise direction
to 180º and increasing negative values in a counterclockwise
direction such that −180º is the same orientation as
+180º.

Although Lead II, with an orientation of about 60º is
the most typical orientation of an axis pointing from atria to
ventricles, it is not abnormal for heart orientation to be
in the range of −30º to +110º — which
can make Leads aVL, AVF, or III rather than Lead II the
primary indicator of normal cardiac depolarization. Thinner
people tend to have a more vertical heart orientation.

The 360º hexaxial reference system defines what is
called the frontal plane of ECG monitoring —
a view of the heart from the front. To provide a view through
the horizontal plane — viewing the heart as
if the body was sliced horizontally through the middle
of the chest — six additional "unipolar"
chest (precordial) leads (designated V1
to V6) are placed on positions of the left
rib cage forming a quarter-circle around the heart. A
quarter-circle on the right rib cage can be used when
it seems more important to monitor the right ventricle
rather than the left ventricle. At birth, T waves are
normally inverted on all precordial leads, but by age 10
only V1 ahd V2 have inverted T waves.

Although Lead V1
typically gives inverted QRS waves (much like Lead aVR),
it is particularly useful to monitor ST−segment changes
and ventricular arrhythmias. Leads V2 to
V4 show particularly abnormal Q waves
and ST−segments when there is blockage of the left
main coronary artery. ST−segment depression in
Leads V2 & V3 can be more
specific to occlusion of the circumflex artery (a branch
of the main left coronary artery). The U wave is most
prominent in Leads V2 & V3,
possibly because these leads are closer to the heart and
have less interference from other organs or
tissues [CIRCULATION; Gerson,MC; 60(5):1014-1020 (1979)].

The ST−segment is a period of diastole between
the end of systole to the beginning of repolarization of the
ventricles. When the ST−segment is normal it is a time
when no depolarization or repolarization is occurring, and
is thus a time of zero potential (flat line at zero). Deviation
(elevation or depression)
of the ST−segment from the baseline is the most common
use of ECG for diagnosis of
ischemia
or infarction —
with the baseline usually defined by the TP−segment.
Extreme ST−segment depression or elevation in
multiple leads generally indicates severe ischemia.
Ischemia or trauma may cause part of
the heart to remain partially or totally depolarized all
of the time — resulting in a potential difference
between the pathologically depolarized tissue and the
normally polarized tissue (ST−segment shift).
Blood flow may be sufficient to maintain life in the
depolarized tissue, although insufficient to result
in repolarization.
Myocardial ischemia can result from increased oxygen
demand (demand ischemia, such as is associated
with exercise or smoking) and/or reduced oxygen
supply (supply ischemia, such as is associated
with anemia or a blocked coronary artery).

ST−segment deviations

ST−segment elevation

ST−segment depression

ST−segment elevation does not necessarily
indicate abnormality, but it can suggest myocardial
injury, such as ventricular aneurism or myocardial
infarction. Pericarditis can cause ST−segment
elevation in all leads. Most athletes have
ST−segment elevation characterized by an upward
concavity in the initial portion of the
ST segment [AMERICAN JOURNAL OF EMERGENCY
MEDICINE; Wu,J; 24(1):77-86 (2006)]. Acute transmural ischemia (injury going
through the entire heart wall) typically causes ST−segment
elevation, often associated with high amplitude T waves.
ST−segment elevation and large T waves are most often
seen in the precordial leads, but may also be seen
in leads I, II, III and aVF if the inferior wall
is ischemic.

ST−segment depression does
not necessarily accompany myocardial ischemia or indicate abnormality.
ST−segment depression is often seen when myocardial ischemia
exists, but can give many false
positives [AMERICAN HEART JOURNAL; Kalaria,VG; 135(5 Pt 1):901-906
(1998)]. A study of patients with coronary
artery disease showed that 66% of ischemic chest pain
episodes were not accompanied by ST−segment depression,
and only 15% of ST−segment depression events
were associated with chest pain (although painful
ischemia is much more closely coupled with
ST−segment depression during high levels of
physical activity) [AMERICAN HEART JOURNAL; Krantz,DS; 128(4):703-712 (1994)].
Changing body positions, hyperventilation, or drinking cold water
causes slight ST−segment depression and T wave
inversion in many normal subjects. Nonetheless,
ST−segment depression can suggest
that myocardial ischemia is delaying the process of
ventricular repolarization, especially if the depression
is horizontal or downsloping. Persons with
left ventricular hypertrophy typically
have ST−segment depression followed by an
inverted T wave. Echocardiography allows for more
precise evaluation of left ventricular size and function.
Hypokalemia causes
ST−segment depression, flattened T waves,
and prominent U waves that can be
larger than the T waves. Ischemia that does not affect
heart tissue from wall-to-wall ("subendocardial
ischemia", ischemia that does not reach to the
endocardium) tends to result
in ST−segment depression [CIRCULATION; Mirvis,PM; 73(2):365-373 (1986)].
ECGs showing ST−segment depression in the absence of
exercise have been shown to be associated with a
two-fold to four-fold increase in cardiovascular
mortality [JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION; Daviglus,ML;
281(6):530-536 (1999) and JOURNAL OF THE AMERICAN COLLEGE
OF CARDIOLOGY; Okin,PM; 45(11):1787-1793 (2005)].

Subendocardial ischemiaST−segment depression

Transmural ischemisST−segment elevation

J point depression and a steep upsloping ST segment
is normal during maximum exercise. But early onset of ST−segment
depression during exercise can be highly indicative of coronary artery disease.
ST−segment depression that is only associated with
exercise is less predictive of cardiovascular disease (many
false positives) than ST−segment depression not associated with
exercise [CIRCULATION; Gianrossi,R; 80(1):87-98 (1989)]. The
sensitivity of ST−segment depression to disease in exercise
increases with the severity of
disease [CIRCULATION; Kligfield,P; 114(19):2070-2082 (2006)].
The test outcome of an ECG taken during exercise (treadmill, bicycle)
is dependent upon when the test is stopped, although exercise
duration itself is not a useful parameter.

Upsloping ST−segment depression is usually not due to a disease condition. In an
exercise stress-test study of asymptomatic middle-aged subjects,
downsloping or horizonal ST−segment depression greater
than one millimeter was predictive of myocardial infarction or
cardiac arrest within eight years, but upsloping or horizontal
ST−segment depression less than one millimeter were
not [CIRCULATION; Rywik,TM; 106(22):2787-2792 (2002)].
The predictive value of upsloping ST−segment depression increases
with the depth of the depression [AMERICAN JOURNAL OF CARDIOLOGY;
Sansoy,V; 79(6):709-712 (1997)]. In exercise stress testing of mostly
coronary artery disease patients, large or moderate reversible ischemic
area was seen in 96% of patients with downsloping ST−segment depression,
80% of patients with horizontal ST−segment depression, and
54% of patients with downsloping ST−segment depression. Large
reversible ischemic area was seen in 62% of patients with downsloping
ST−segment depression, 26% horizontal, and 20%
upsloping [ANNALS OF NONINVASIVE ELECTROCARDIOLOGY; Polizos,G;
11(3):237-240 (2006)]. In addition to area, intensity of ischemia &
intraventricular conductance also affect ST−segment
depression [CIRCULATION; Kligfield,P; 114(19):2070-2082 (2006)].

Correlation of ST−segment depression with heart rate greatly
improves the predictive value of exercise-induced
ST−segment depression for cardiovascular disease.
Inclusion of ST−segment depression with heart rate
during the first minute of recovery after exercise
(ST/HR hysteresis) further improves the predictive value of
ST−segment depression [CIRCULATION; Kligfield,P; 114(19):2070-2082 (2006)].
The ST/HR hysteresis method of exercise ECG testing has
been shown to be predictive of a more than 3-fold risk of
coronary heart disease events in a Framingham
study [CIRCULATION; Okin,PM; 83(6):866-874 (1999)]. Lead V5
is reportedly the most important lead in detecting coronary heart
disease using ST/HR hysteresis [JOURNAL OF ELECTROCARDIOLOGY; Viik,J;
32(Suppl):70-75 (1999)].

High variation in the amplitude & shape of the ST segment & T wave
is a significant indicator of sudden cardiac death risk [HEART RHYTHM;
Verrier,RL; 6(3):416-422 (2009)].